Chlamydia pneumoniae infection impairs endothelium‐dependent relaxation in an ex vivo porcine coronary artery model

Chlamydia pneumoniae (Cpn) infection is associated with the development of atherosclerosis. The current study aims to determine whether Cpn infection can initiate endothelial dysfunction in the absence of a host immune response. Isolated porcine coronary arteries were administered 1 of 3 treatments: live Cpn, heat‐inactivated Cpn (mock infection), no treatment (control). Relaxation responses to bradykinin (Bk) and sodium nitroprusside were measured at days 0, 5 and 10 post‐infection (pi). At day 10 pi, Cpn infected vessels displayed decreased BK‐induced relaxation responses of 60% and 54% compared to control and mock‐infected vessels, respectively. These changes were accompanied by a significant decrease in endothelial nitric oxide synthase (eNOS) protein expression in Cpn infected vessels compared to the other groups. Dihydroethidium staining of coronary cross‐sections revealed an increase in superoxide production in Cpn infected vessel compared to mock‐infected and control vessels. Protein expression of p22phox was upregulated in both Cpn and mock infected vessels compared to control vessels. Our results demonstrate that Cpn infection alone can contribute to endothelial dysfunction by reducing nitric oxide production and increasing oxidative stress. (Supported by Canadian Institutes of Health Research)